Critical opening pressure and reactivity of tail vessels in conscious hypertensive rats

1976 ◽  
Vol 54 (3) ◽  
pp. 314-321
Author(s):  
A. C. Darke ◽  
P. G. Nair ◽  
P. Gaskell
Keyword(s):  
Blood Pressure ◽  
Renovascular Hypertension ◽  
Vascular Reactivity ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Opening Pressure ◽  
Critical Opening ◽  
Resistance Vessels ◽  
Before And After ◽  
Desoxycorticosterone Acetate

The possible role of increased vascular reactivity in the mechanism of experimental hypertension was studied by measurements of the critical opening pressure (COP) of tail vessels in conscious rats. In hypertension induced by administration of desoxycorticosterone acetate (DOCA) and replacement of the drinking water by 1% NaCl solution (DOCA–NaCl hypertension), and in one-kidney Goldblatt renovascular hypertension, the raised level of blood pressure was associated with an increased COP of the tail vessels when measured both before and after ganglionic blockade. In rats treated with either DOCA alone or 1% NaCl alone there was no significant increase in systolic blood pressure (SBP) or COP relative to the corresponding controls. In all four experimental series intravenous infusion of angiotensin or norepinephrine in conscious ganglion-blocked rats produced dose-dependent increases in SBP and COP. In DOCA–NaCl hypertensive rats but not in renovascular hypertensives, nor in rats treated with DOCA alone or 1% NaCl alone, the increase in COP for a given increment in dose of angiotensin or norepinephrine was significantly greater than in the control rats. It is concluded that in DOCA–NaCl hypertension there is a true increase in the reactivity of the smooth muscle of the resistance vessels to angiotensin and norepinephrine. In renovascular hypertension this is not the case and other factors must therefore be involved in causing the increased blood pressure and COP.

Abstract 343: Vascular Inflammation in Two Rat Models of Arterial Hypertension is Promoted by Coagulation FXI

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Jeremy Lagrange ◽  
Sabine Kossmann ◽  
Andreas Daiber ◽  
Matthias Oelze ◽  
Brett Monia ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Hypertension ◽  
Feedback Loop ◽  
Thrombin Generation ◽  
Vascular Reactivity ◽  
Platelet Rich Plasma ◽  
Vascular Dysfunction ◽  
Vascular Inflammation ◽  
Critical Role ◽  
Experimental Hypertension

Backgroud: Interactions of platelets, leukocytes and the vessel wall play pivotal roles in activating coagulation and precipitating thrombosis. We were recently able to uncover an angiotensin II (ATII) driven factor XI (FXI)-thrombin amplification loop leading to vascular injury in experimental hypertension in mice. Objective: We wanted was to explore the role of thrombin-FXI feedback loop in different models of arterial hypertension in rats. Methods: ATII treated wistar rats (1mg·kg -1 ·d -1 for 7 days using osmotic minipumps) and 5/6 nephrectomized were used for this study. During 2 weeks rats were treated with a FXI antisense oligonucleotide (ASO) (1 week after nephrectomy or 2 weeks before ATII pump implantation, respectively). Blood pressure was recorded with tail cuff measurement. Fluorescence oxidative microtopography was used to evaluate vascular ROS production. Vascular reactivity was assessed in isolated aortic segment. Calibrated automated thrombography was used to measure thrombin generation. Results: In ATII infused rats as well as 5/6 nephrectomized rats vascular dysfunction related to hypertension was attenuated when rats were treated with FXI ASO. Hypertension induced VCAM-1 expression was normalize with inhibition of FXI. ROS formation was normalized in ATII infused rats as well as 5/6 nephrectomized treated with FXI ASO. Thrombin generation in platelet rich plasma from 5/6 nephrectomized rats was completely abolished when FXI was inhibited. Finally the overall blood pressure increase was abrogated by FXI ASO treatment in 5/6 nephrectomized rats. Conclusion: FXI plays a critical role in a FXI-thrombin feedback loop in hypertension. This pathway is relevant in mice and rats and we were able to very recently obtain the first conclusive results in humans. FXI could be a novel therapeutic target to interrupt this heterotypic cellular coagulation-inflammatory circuit.

Renin content and excretory function of the kidney in rats with experimental hypertension

1962 ◽  
Vol 202 (4) ◽  
pp. 795-799 ◽  
Author(s):  
H. Brunner ◽  
P. A. Desaulles ◽  
D. Regoli ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Hypertension ◽  
Experimental Hypertension ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Excretory Function ◽  
Contralateral Kidney ◽  
Ligation Of The Ureter ◽  
Renin Content

To determine relationship between kidney renin content and excretory function, rats with renal hypertension induced by unilateral clamping of the renal artery were given an oral load of 3 ml of 0.9% saline/100 g body wt. Excretion of the saline load was accelerated in rats with renal hypertension as well as in animals with hypertension due to overdosage with cortexone and salt, provided that the loading experiment was made 3–4 weeks after hypertension was established, but not when animals had been hypertensive for 11–14 weeks. Renin concentration was markedly reduced in the unclamped kidney and also in the kidney of the rats overdosed with cortexone and salt. Excreting capacity of the clamped kidney was compared with that of the unclamped kidney, after removal or after functional elimination of the contralateral kidney, by ligation of the ureter, 3, 24, and 48 hr after the operation. In all experiments excretion of saline load by the unclamped kidney was more rapid than by the clamped kidney, but the highest values were reached in the presence of a functional clamped kidney. Only in rats with elevated blood pressure was the load more rapidly excreted than in normal rats, but hypertension alone cannot be the only factor responsible, the excretion not being accelerated in unilaterally nephrectomized hypertensive rats. Although these hint at a connection between the renin concentration and renal function the nature of this relationship remains uncertain.

Effects of aldosterone on blood pressure and glucose-6-phosphate dehydrogenase activity of heart muscle

1969 ◽  
Vol 47 (2) ◽  
pp. 193-197 ◽  
Author(s):  
C. C. Liew ◽  
A. G. Gornall
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Heart Muscle ◽  
Specific Activity ◽  
Systolic Pressure ◽  
Experimental Hypertension ◽  
Low Doses ◽  
Significant Elevation ◽  
Desoxycorticosterone Acetate ◽  
Glucose 6 Phosphate Dehydrogenase

A study was made of the effects of aldosterone on the activity of heart muscle glucose-6-phosphate dehydrogenase (G6PDH) in relation to the pathogenesis of experimental hypertension. In a 17-day experiment, with rats given daily 1-μg doses of aldosterone/100 g body weight, no change in systolic pressure occurred and the specific activity (s.a.) of heart muscle G6PDH declined. Rats receiving daily 100 μg of aldosterone, or 500 μg of desoxycorticosterone acetate (DOCA) per 100 g body weight, showed a significant elevation of systolic pressure by the 17th day. This effect was accompanied by increases in the s.a. of heart muscle G6PDH, apparently preceding the development of hypertension. Evidence for a homeostatic role for aldosterone was revealed by the ability of low doses to prevent a decline in s.a. of cardiac G6PDH during fasting, and to reverse the increase produced by DOCA.

Cardiopulmonary reflexes and blood pressure in exercising sinoaortic-denervated dogs

1984 ◽  
Vol 57 (5) ◽  
pp. 1417-1421 ◽  
Author(s):  
D. A. Daskalopoulos ◽  
J. T. Shepherd ◽  
S. C. Walgenbach
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vagal Afferents ◽  
Systemic Resistance ◽  
Vigorous Exercise ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Cardiopulmonary Receptors

To examine the role of cardiopulmonary receptors in arterial blood pressure regulation during and after exercise, conscious dogs with chronic sinoaortic denervation were subjected to 12 min of light exercise and 12 min of exercise that increased in severity every 3 min. Hemodynamic measurements were made before and after interruption of cardiopulmonary afferents by bilateral cervical vagotomy. During both exercise protocols, after an initial transient decrease, the arterial blood pressure remained close to resting values before and after vagotomy. On cessation of the graded exercise, the arterial blood pressure did not change before, but a rapid and sustained increase in pressure occurred after vagotomy. At the time of this increase the cardiac output and heart rate were returning rapidly to the resting level. The study demonstrates that in the chronic absence of arterial baroreflexes, vagal afferents prevent a rise in arterial blood pressure after vigorous exercise presumably by the action of cardiopulmonary receptors causing a rapid dilatation of systemic resistance vessels.

Thromboxane A2-prostaglandin H2 and renovascular hypertension in rats

1994 ◽  
Vol 267 (5) ◽  
pp. R1190-R1197 ◽  
Author(s):  
E. H. Boussairi ◽  
J. Sacquet ◽  
J. Sassard ◽  
D. Benzoni
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Receptor Antagonist ◽  
Renovascular Hypertension ◽  
Vascular Reactivity ◽  
Thromboxane A2 ◽  
Malignant Hypertension ◽  
Receptor Blockade ◽  
Vascular Responsiveness ◽  
Goldblatt Hypertension

To evaluate the contribution of thromboxane (Tx) A2-prostaglandin (PG) H2 in two-kidney, one-clip Goldblatt hypertension (GH), 26 GH rats were chronically treated (GHT) with a specific TxA2-PGH2 receptor antagonist, CGS-22652 (30 mg.kg-1.24 h-1 sc); 28 others as well as 17 sham-clipped (SC) rats received vehicle. Twelve GH and 3 GHT rats developed malignant hypertension and died. After 6 wk of treatment, GH rats exhibited higher mean blood pressure (BP; 189 +/- 3 vs. 118 +/- 2 mmHg) and an increased vascular reactivity to the main pressor agents compared with SC rats. Chronic TxA2-PGH2 receptor blockade lowered mean BP in 13 GHT rats (125 +/- 3 mmHg) and decreased their vascular reactivity compared with GH rats. However, 10 GHT rats remained hypertensive (190 +/- 9 mmHg) and differed from the former by an increased vascular reactivity to vasopressin. It is concluded that renal artery clipping induces either benign or malignant hypertension. In benign forms, TxA2-PGH2 blockade normalizes BP through decreasing the vascular responsiveness to the main pressor agents. In malignant forms, it limits the elevation of BP and markedly reduces mortality.

The effect of repeated cold exposure of the hand on the reactivity of digital vessels

1969 ◽  
Vol 47 (3) ◽  
pp. 261-265 ◽  
Author(s):  
Peter Gaskell ◽  
Kathleen L. Long
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Cold Exposure ◽  
Opening Pressure ◽  
Relative Flow Rate ◽  
Opposite Hand ◽  
Critical Opening ◽  
Before And After ◽  
Relative Change ◽  
Relative Flow

One hand of each of 10 subjects was immersed in stirred water at 4 °C for 1 h per day, 5 days per week, for 3 weeks, to produce local acclimatization to cold. The opposite hand was immersed at the same time in water at 32 °C. The reactivity of digital vessels in a finger of each hand was measured as the increase in the critical opening pressure of the vessels in response to an intravenous infusion of noradrenaline at 2 and 5 μg/min. The reactivity of digital vessels in the test hand was compared with that in the control hand both before and after the repeated cold exposure of the test hand to see whether the cold exposure altered the reactivity of vessels in the test hand relative to that in the control hand. No evidence of such a relative change was obtained. Resting blood flow at 21 and 32 °C in the test hand was compared with that in the control hand both before and after the repeated cold exposure. No change in the relative flow rate in the two hands was observed as a result of the cold exposure. Roentgen studies of the hands did not reveal any effect of the repeated cold exposure on the mineralization of the bones of the hands.

Bile acids are able to reduce blood pressure by attenuating the vascular reactivity in spontaneously hypertensive rats

Life Sciences ◽  
1988 ◽  
Vol 42 (19) ◽  
pp. 1861-1868 ◽  
Author(s):  
Takehiko Tominaga ◽  
Hiromichi Suzuki ◽  
Yasuhide Ogata ◽  
Toshio Imafuku ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Bile Acids ◽  
Spontaneously Hypertensive Rats ◽  
Vascular Reactivity ◽  
Reduce Blood Pressure ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive
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